Sheep Versican ELISA, VCAN
- Known as:
- Sheep Versican Enzyme-linked immunosorbent assay test, VCAN
- Catalog number:
- E14V0050
- Category:
- -
- Supplier:
- Blue Gene Biotech
- Gene target:
- Sheep Versican ELISA VCAN
Related genes to: Sheep Versican ELISA, VCAN
- Gene:
- VCAN NIH gene
- Name:
- versican
- Previous symbol:
- CSPG2
- Synonyms:
- PG-M
- Chromosome:
- 5q14.2-q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-18
- Date modifiied:
- 2018-02-13
Related products to: Sheep Versican ELISA, VCAN
Related articles to: Sheep Versican ELISA, VCAN
- Salmon skin, a high-volume by-product of seafood processing, offers a circular-bioeconomy route to sustainable, value-added ingredients. This study aimed to generate low-molecular-weight collagen peptides (LMWCPs) from salmon skin using a stepwise enzymatic process and to evaluate their safety and pro-extracellular-matrix (ECM) activity in human BJ fibroblasts. LMWCPs were produced by sequential hydrolysis (alcalase/papain, then collagenase) and characterized as low-molecular-weight peptide preparations with a mean dispersed particle diameter of approximately 117 nm. LMWCPs display negatively charged peptide dispersions with a mass centered around ~1 kDa. Cytocompatibility (MTT) showed no toxicity up to 1.5 mg/mL over 48 h. Gene expression by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) revealed a robust, dose-dependent ECM response: collagen type I alpha 1 chain (COL1A1) increased by approximately 7-fold, with additional rises of 5-6-fold in versican (VCAN) levels and modest increases in elastin (ELN) and transforming growth factor-β (TGF-β). These findings provide an exploratory process-to-phenotype link between the two-step hydrolysis process, physicochemical characteristics of the resulting LMWCPs, and changes in ECM-related gene expression in BJ fibroblasts. Overall, this study demonstrates that salmon skin LMWCPs were cytocompatible within the tested concentration range and modulated several ECM-related genes, providing a preliminary basis for future protein-level, functional, and translational evaluation. - Source: PubMed
Publication date: 2026/09/11
Benjakul SoottawatNilsuwan KrisanaPatil UmeshHaewphet ThaiyawatSaetang Jirakrit - Three transcriptomic cohorts, GSE30528, GSE96804, and GSE104948, comprising 62 DKD and 59 control samples, were integrated for differential expression and weighted gene co-expression network analyses. Candidate genes were prioritized using disease databases, protein-protein interaction analysis, 113 machine-learning algorithm combinations, and SHAP analysis. Model performance was evaluated in GSE30529 and GSE99339. The prioritized genes were then subjected to reverse network pharmacology, followed by FN1 validation in GSE47184 and surface plasmon resonance (SPR). An independently generated mouse single-cell RNA-sequencing dataset comprising 36,819 cells from three DKD and three control mice was subsequently used to localize Fn1 expression. Finally, db/db mouse experiments and an Fn1-overexpression rescue experiment in high-glucose-treated mesangial cells were performed. - Source: PubMed
Publication date: 2026/09/09
Li YiminTian YuqingWu ZhenhuaXia FangyuZheng LiyifanRen MeifangZhao MeijiaoZhang QianTan JinchuanXu QingyouYang Fengwen - Periodontitis (PD) and systemic juvenile idiopathic arthritis (sJIA) are chronic inflammatory diseases with potential clinical links, yet their shared molecular mechanisms remain unclear-patients with JIA face elevated periodontal risk, the temporomandibular joint affected in JIA shares inflammatory pathways with PD, Th17 cells drive both conditions, and glucocorticoid therapy may exacerbate periodontal vulnerability. This study aimed to explore the shared mechanisms and potential therapeutic targets of PD and sJIA using genetic expression data from the GEO database and performed comprehensive bioinformatics analyses, including differential expression gene analysis, weighted gene co‑expression network analysis (WGCNA), functional enrichment analysis, protein‑protein interaction network construction, and machine learning across 175 predictive models with the Ridge + AdaBoost ensemble identified as the best‑performing combination, followed by SHapley Additive exPlanations (SHAP) for model interpretability, CIBERSORT for immune infiltration assessment, and molecular docking with 100‑ns molecular dynamics simulations for therapeutic target validation. We identified 37 shared candidate genes between PD and sJIA, which were significantly enriched in IL‑17, NF‑κB, rheumatoid arthritis, and lipid atherosclerosis pathways, and machine learning screening further selected six core diagnostic genes (FAM46C, CXCL1, SELP, LGALSL, ELOVL4, VCAN), with SELP demonstrating the most robust cross‑model, cross‑dataset diagnostic value (AUC > 0.8); SHAP analysis confirmed SELP as a stable risk‑driving predictor across all models, while CXCL1 consistently showed protective effects. Immune infiltration revealed shared neutrophil elevation and CD8 ⁺ T‑cell reduction, with conserved CXCL1 and SELP correlations with neutrophils and resting mast cells, and FAM46C with plasma cells.Drug‑target network analysis identified IL1B, MMP1, and ITGAM as core targets, and molecular docking yielded strong binding affinities for deoxycholic acid-MMP1 (-7.6 kcal/mol), kaempferol-IL1B (-7.2 kcal/mol), kaempferol-ITGAM (-6.9 kcal/mol), with MD simulations confirming stable and specific binding. Collectively, this study explores shared genetic and immunological characteristics between PD and sJIA, suggests that SELP may serve as a critical cross‑disease diagnostic biomarker, and offers novel insights into their pathogenesis and potential therapeutic targets that warrant further experimental validation. - Source: PubMed
Publication date: 2026/09/23
Deng QingaoWang JunjieWang XingQi Lu - This study investigated whether 5-oxoproline, a key metabolic intermediate in the gamma-glutamyl cycle, improves the maturation and developmental competence of low-quality porcine cumulus-oocyte complexes (COCs) during in vitro maturation (IVM). High-quality grade A COCs were used as the positive control (PC), whereas low-quality grade B COCs served as the negative control (NC) or were cultured for 44 h in IVM medium supplemented with 5-oxoproline. Among the concentrations tested, 500 μM 5-oxoproline most effectively restored nuclear maturation in grade B oocytes to a level comparable with that of the PC group. This treatment significantly reduced intracellular reactive oxygen species, increased intracellular glutathione (GSH) levels, and rescued cumulus cell expansion. Quantitative real-time PCR analysis demonstrated that 5-oxoproline upregulated the antioxidant-related gene TXN and cumulus expansion-associated genes, including HAS2, PTGS2, and VCAN, while reducing the sustained overexpression of the hyaluronan receptor CD44 toward PC baseline levels. Functionally, 5-oxoproline supplementation enhanced the developmental competence of grade B oocytes as demonstrated by increased blastocyst formation after both parthenogenetic activation and in vitro fertilization. These findings suggest that 5-oxoproline improves the quality of compromised porcine oocytes by restoring redox homeostasis, supporting cumulus matrix remodeling, and enhancing subsequent embryo development. 5-Oxoproline may therefore represent a useful metabolic supplement for improving the efficacy of porcine in vitro embryo production. - Source: PubMed
Publication date: 2026/09/14
Kim SeeunHa YunjuLee SeungjunBack GunwooBilal MuhammadKim Min JungCho Jongki - Viral and bacterial lung infections place a significant burden on public health. Versican, an extracellular matrix (ECM) chondroitin sulfate proteoglycan, coordinates the innate immune response in multiple experimental models. Versican's potential as an immunomodulatory molecule makes it a promising therapeutic target for controlling the host's immune response to lung infection. However, versican's contribution to lung inflammation, injury, and immune cell activity during influenza A virus (IAV) infection represents a critical knowledge gap. To address our central hypothesis that mesenchymal-derived versican is pro-inflammatory and enhances the innate immune response to IAV infection, we generated a tamoxifen-inducible mouse deficient in mesenchymal-derived versican (B6. Col1a2-Cre/Vcan, Col1a2/Vcan). We report that mesenchymal-derived versican plays a critical role in neutrophil, monocyte, and dendritic cell migration into the lungs and airways early in IAV infection. Intriguingly, mesenchymal-derived versican deficiency had the most substantial negative impact on neutrophil emigration into the lungs. We found that neutrophils were less adhesive to the ECM of Col1a2/Vcan mouse lung fibroblasts (mLFs), which had a significant decrease in versican compared to wild-type mLFs. Additionally, Col1a2/Vcan mLFs treated with poly(I:C) have reduced cell-associated hyaluronan. These findings suggest that fibroblast-derived versican is necessary for adhesion to lung fibroblasts by neutrophils as they transit into the lung interstitium and airways from the pulmonary vasculature. Our findings demonstrate that mesenchymal-derived versican is a key regulator of the early host immune responses to IAV. - Source: PubMed
Publication date: 2026/09/16
Brune Jourdan EChang Mary YTang FengyingLopez-Martinez CeciliaReeves Stephen RChan Christina KWaldron PeterBoyd David FGharib Sina AThomas Paul GAltemeier William AFrevert Charles W